Certain common bacterial immunogens in the rumen can produce large amounts of lactic acid. These include but are not limited to Streptococcus bovis and Lactobacillus spp. As the host consumes starch in the diet, these deleterious organisms produce very high amounts of lactic acid that can result in reduced performance and, in acute situations, dangerously low pH rumen levels. Once the pH lowers in the rumen, these bacterial species become the primary etiologic agents in rumen abscesses.
Lactic acid acidosis is produced in ruminants fed diets high in grain. These grain-fed animals are subject to a number of nutritional or metabolic problems, but most are secondary to acute acidosis. Lactic acidosis occurs when there is an abrupt increase in the intake of readily fermentable carbohydrates. A typical example would occur when range or pasture fed cattle, which may never have been fed grain in their lives, are brought into a feedlot and fed grain. If the amount of grain fed exceeds the ability of the rumen microbial population to move in an orderly transition from primary cellulite based to a starch-based diet, there is a shortage of amylolytic organisms. The void is quickly occupied by a fast growing amylolytic bacteria, Streptococcus bovis, which grows rapidly and produces lactic acid as a fermentation end product, particularly D-lactate which is poorly absorbed and metabolized. Lactobacillus spp. also produces lactate. As S. bovis increases, the rumen pH drops, causing spiraling accumulation of lactic acid in the rumen and a consequent lower pH. The accumulation of lactic acid in the rumen and blood causes rumen acidosis and metabolic acidosis. This has a corrosive affect on the rumen wall and causes the papillae to peel off. Absorption is impaired and bacteria inside the rumen wall can gain system entrance. A high incidence of liver abscesses can result. Additionally, lower rumen pH can inhibit the growth of all organisms, including beneficial microbes that aid in efficient feed digestion.
Chronic liver abscesses reduce growth rates, feed efficiency, and carcass dressing percentage. The incidence of liver abscess in feedlot cattle is 12-32%. It is a major economic import because of carcass condemnation and reduced animal performance. These ruminal lesions foster an invasion of bacterium, principally Fusobacterium necrophorum. It is generally accepted that the rumen lesions resulting from acidosis are the predisposing factors for liver abscesses. F. necrophorum prosseses a number of virulent factors that allow the organism to enter and colonize the rumen epithelium and subsequently enter and establish an infection in the liver.
The accumulation of lactic acid in the rumen increases the osmolotity of the rumen, drawing water from the blood into the rumen and causing dehydration. Recovery at this stage is unlikely. Absorbed acid may cause systematic acidosis with a lowered blood pH, electrolyte imbalance, and lead to kidney failure.
Acute lactic acidosis causes dramatic increases in rumen acidity and osmololity causing severe rumenity. Decreased blood pH, fatal dehydration, and chronic acidosis reduce feed intake and animal performance in feedlot cattle and dairy cattle.
Acidosis is not readily treated but best prevented. Antibiotics can be used to contain S. bovis and Lactobacillus spp.
Normally the rumen environment is anaerobic with pH of approximately 6.5. Rumen pH levels between 5.2 and 5.6 define sub-acute acidosis. Acute acidosis is when the rumen pH level dips below 5.2. The use of monensin, a feed additive marketed under the name Rumensin, has potential to improve health and production of dairy on high concentrate diets but not fully prevent ruminal acidosis. In many dairy operations, the challenge is not with acute but sub-clinical acidosis. Monensin, however, is not cleared for use in lactating dairy cows
The cascade effects of acidosis originating from the initial ingestion of carbohydrate depend upon the intensity and duration of the insult. The most critical is the pH threshold. This relates to microbial growth rates and shifts in ruminal population, and significantly influences the systemic metabolic state.
A principal objective of the present invention is to substantially prevent the colonization of deleterious organisms such as S. bovis, Lactobacillus spp. and F. necrophorum, as well as the growth of such organisms in the rumen and the intestinal tracts of food animals resulting in their substantial elimination from the animal by the administration of fowl egg antibody to the specific organisms.
Haptens are partial or incomplete immunogens such as certain toxins, which cannot by themselves cause antibody formation but are capable of combining with specific antibodies. Such haptens may include bacterial toxin, yeast mold toxin, viruses, parasite toxins, algae toxins, etc.
Under the most popular current feeding system, food animal feed efficiency is enhanced through the use of ionophores such as monensin, a feed additive marketed under the trade name Rumensin. This is a class of polyester antibiotics approved for feed given to beef cattle and diary heifers, but is not approved for use with lactating dairy cattle. Most gram-positive microorganisms are non-specifically vulnerable to the ionophores, antibiotics that can be quite toxic to the host animal if used improperly. As these antibiotics are not specific, many of the ruminal microorganisms required to digest the cellulose of ingested plant material may also be affected. The problem with carry over and development of resistant strains of microorganisms are also of major concern to the industry. The use of broad-spectrum antibiotics has further drawbacks including vulnerability to human error, additional cost, consumer resistance, and the like. In addition, the monensin type additive cannot be added with the commonly used molasses-based supplements.